Abstract:Aim To observe the effect of high glucose on the expression and activity of thrombomodulin in human umbilical vein endothelial cells （HUVEC）. Methods HUVEC were incubated in vitro, sub-experiment: ①control group ②10 mmol/L glucose group ③20 mmol/L glucose group, all incubated for 24 h. Flow cytometric and RT-PCR technique were used for detecting thrombomodulin protein and mRNA, respectively. Microplate Reader was used for detecting thrombomodulin activity. Results Compared with control group, both mRNA （2.05±0.19、1.44±0.32 vs 1）and protein （41.38±3.41、32.60±2.59 vs 27.96±1.58） levels of thrombomodulin increased in 20 mmol/L glucose group and 10 mmol/L glucose group （P<0.05） and the thrombomodulin activity enhanced （0.4157±0.0129 vs 0.3957±0.0100，P<0.05） in HUVEC of 20 mmol/L glucose group. Conclusion Exposure to high glucose increased the expression of thrombomodulin and enhanced the thrombomodulin activity in HUVEC. The upregulation of thrombomodulin in HUVEC cultivated in high glucose conditions may represent a defense mechanism against the stress.

Abstract:Aim To investigate the role of calcium- calmodulin dependent kinaseⅡand calcineurin in tumor necrosis factor α（TNF-α）-induced cardiomyocyte hypertrophy through Phosphatidylinositol 3-kinase pathways. Methods Intracellular free Ca²⁺ concentration was measured by laser confocal microscopy. The protein content was assayed with Lowry’s method. The cardiomyocytes volumes were measured by computer photograph analysis system. The expression of CaMKⅡδB and CaN was determined by western blot. Results ①LY294002, a selective PI3K inhibitor, significantly suppress the elevation of intracellular free Ca²⁺ concentration induced by TNF-α in cultured ventricular myocytes from the neonatal rat. The effect was similar to that of LY294002+2-APB（P>0.05）, but lower than LY294002+ryanodine（P<0.05）. ②LY294002 significantly reduced the enhancements in protein content and cell size induced by TNF-α. The effect was similar to that of 2-APB+LY294002, but higher than 2-APB and lower than ryanodine+LY294002. LY294002, a PI3K inhibitor, suppressed the expression of CaMKⅡδB and CaN induced by TNF-α in myocytes which was similar to that of LY294002+2-APB. Conclusion TNF-α induced cardiac hypertrophy through activing PI3-kinase pathway in cultured ventricular myocytes from the neonatal rat, which was mediated partly by IP3R to mediate expression of CaMKII and calcineurin through increasing the intercellular Ca²⁺.

Abstract:Aim To investigate the influences of 3 kinds of traditional Chinese herbal compound drug serum Sijunzi decoction （SD）, Xuefu Zhuyu decoction （XZD） and Buyang Huanwu decoction （BHD） on the expression of lectin-like oxidized low density lipoprotein receptor-1 （LOX-1）, tumor necrosis factor-α （TNF-α）, vascular cell adhesion molecule-1 （VCAM-1） and intercellular adhesion molecule-1 （ICAM-1） induced by lipopolysaccharide （LPS） in human umbilical vein endothelial cell （HUVEC）, and to explore the mechanism of traditional Chinese medicine compound preventing and treating atherosclerosis. Methods For cell experiment, SD, XZD, BHD containing drug serums and normal blank serum were prepared by using drug serological method. HUVECs were cultured in vitro and divided randomly into 6 groups: blank control group, model group, atorvastatin group, SD group, XZD group and BHD group. HUVECs were stimulated with LPS for 2 h, then treated separately with atorvastatin and traditional Chinese herbal compound drug serum for 24 h. The mRNA and protein expressions of LOX-1, TNF-α, VCAM-1, and ICAM-1 were detectd by fluorescence quantitative PCR and Western blot. Results mRNA and protein expressions of LOX-1, TNF-α, VCAM-1 and ICAM-1 were significantly increased after HUVEC stimulated by LPS （P<0.01）. mRNA and protein expressions of LOX-1, TNF-α, VCAM-1 and ICAM-1 were significantly inhibited, after adding respectively XZD, BHD containing drug serums and atorvastatin to intervene （P<0.05）. But SD containing drug serum had no significant effect （P>0.05）. Conclusions Traditional Chinese herbal compound XZD and BHD can inhibit the expressions of inflammatory factors LOX-1, TNF-α, VCAM-1 and ICAM-1, and this may be one of the mechanisms of them to prevent and treat atherosclerosis. While SD has no such role.

Abstract:Aim To explore the controlled release effect of the recombinant Ephrin-b2/Fc chimera from self assembling peptide of RAD16-Ⅱ and the immunogenicity of RAD16-Ⅱ. Take RAD16-Ⅱas a delivery vehicle to prevent the ungroomed Ephrin-b2/Fc protein from being degraded in vivo and increase therapeutic effect. Methods The moulding of the oligopeptide was observed by macroscopy and microscopy. The releasing effect was assayed by releasing curve obtained from test in vitro. In vivo, Sprague-Dawley rats were prepared to acute myocardial infarction models by ligation of the left anterior descending branch. The survival rats were divided into 2 groups and separately intra myocardially injected recombinant Ephrin-b2/Fc proteins（E group，n25） and sapeptide- Ephrin-b2/Fc protein complex（ES group，n25）. At set time（1 h,3 h,24 h,7 d,14 d），the samples of the myocardial tissue and sera were collected and respectively used for immunofluorescence and westernblot to determine the remaining or losing of the protein. RAD16-Ⅱ solution was administrated through subcutaneous injection. 5 weeks later, the titer of anti-sapeptide in serum was assayed by ELISA. Results It is observed that RAD16-Ⅱsolution can self-assemble into nanofibers which fabricate net structure in condition of PBS. Within net structure, the releasing duration of chimeric Ephrin-b2/Fc lasted up to 144 h and more than 50% mass was released in 120 h. As shown in immunofluorescence, the retention duration of the chimeric protein in ES group was significantly longer than that in E group at the same time（P<0.05）. And westernbolt also demonstrated the amount of protein releasly into blood in ES group was less significant than that in E group（P<0.05）. The titer of the antibody was not significantly different from RAD16-Ⅱ administration to negative control group, which showed that RAD16-Ⅱ would not trigger immune response. Conclusion RAD16-Ⅱ oligopeptide can postpone the release of chimeric Ephrin-b2/Fc both in vivo and in vitro. It is a relatively reliable and safe biomaterial delivery vehicle of Ephrin-b2/Fc protein in myocardial infarction and ischemia research.

Abstract:Aim To explore the effect and potential mechanisms of simvastatin pretreatment on neurogenic pulmonary edema （NPE） in rats. Methods The SD rats were randomly divided into control group, NPE group, simvastatin 20 mg group and simvastatin 40 mg group. The rats in the simvastatin group were pretreated with simvastatin for 4 weeks according to 20 mg/（kg·d） and 40 mg/（kg·d） by intragastric administration, respectively. The NPE models of rats except the control group were induced by cerebellomedullary cistern puncture after pretreatment of 4 weeks. The 24 h survival rates of rats were evaluated by Kaplan-Meier method. At 6 h following operation, the severity of pulmonary edema, lung tissue pathological changes of rats were evaluated by Wet Dry proportion method and HE staining, respectively. The apoptosis rate, protein and mRNA expressions of Bcl-2 and Bax of primary cultured PMVEC were detected by flow cytometry, Western blot and RT-PCR, respectively. Results Compared with the control group, the Wet Dry proportion of lung increased significantly, and the pulmonary interstitial edema and alveolar edema of the rats were obvious by HE staining and the apoptosis rate of PMVEC increased significantly at 6 h following operation in the NPE group. The 24 h survival rates of rats in the NPE group decreased significantly. The protein and mRNA expressions of Bcl-2 of PMVEC were downregulated, but the protein and mRNA expressions of Bax were upregulated in the NEP group. While the severity of pulmonary edema and survival rates of the 20 mg/（kg·d） simvastatin pretreatment rats decreased significantly when compared with that of rats in the NPE group. And the apoptosis rate of PMVEC decreased in the 20 mg/（kg·d） simvastatin pretreatment rats. The protein and mRNA expressions of Bcl-2 in the PMVEC were upregulated but the protein and mRNA expressions of Bax were downregulated in the simvastatin pretreatment rats. When compared with the 20 mg/（kg·d） simvastatin pretreatment rats, these parameters changes more significantly in the 40 mg/（kg·d） simvastatin pretreatment rats. Conclusions The study shows that simvastatin pretreatment decreases the severity of NPE and improves survival rate of rats. One of the mechanisms may decrease the apoptosis rate of PMVEC through upregulating the expression of Bcl-2 and downregulating the expression of Bax. It is implied that simvastatin may play a role in the prevention and treatment of NPE, but it needs to be further confirmed by clinical researchs.

Abstract:Aim To improve the method of making myocardial infarction models in dogs and to form transmural myocardial infarction. Methods 16 healthy adult mongrel dogs were randomly divided into control group （n＝8） and experimental group （n＝8）. The myocardial infarction was established. In control group, the left anterior descending coronary artery was ligated. While in experimental group, the left anterior descending coronary artery and first diagonal branch were ligated. After 6 weeks, cardiac general morphology and histopathology were observed. Results After 6 weeks, there were 6 dogs survived in control group and 5 dogs survived in experimental group, and the survival rates were 75.0% and 62.5% respectively. There was no statistically significant difference at survival rate in two groups （P＝0.590）. Of the survived 6 dogs in the control group, there were 2 dogs that myocardial infarction could be seen clearly by cardiac general morphology and histopathology Of the other 4 dogs, there was no myocardial infarction by cardiac general morphology, but micro-infarction was observed by histopathology. Of the survived 5 dogs in the experimental group, myocardial infarction could be observed clearly by cardiac general morphology and histopathology in all dogs. There was significant difference in the dog number of transmural myocardial infarction in two groups （P＝0.022）. Conclusion The ligation of the left anterior descending coronary artery and first diagonal branch in dog can form transmural myocardial infarction, which is an effective and reliable method for preparation of myocardial infarction model.

Abstract:Aim To observe the change of activation of myocardial NF-κB and its downstream inflammatory factors such as tumor necrosisfactor-alpha（TNF-α）, whiteinterleukin-1β（IL-1β）and whiteinterleukin-6（IL-6） after myocardium ischemia reperfusion in diabetic rat and its mechanism. Methods 74 healthy male Sprague-Dawley rats were randomly divided into diabetics group（n50） and non-diabetics group（n24）. Experimental diabetes was induced in the animals by a single intraperitoneal administration of STZ dissolved in 0.1 mol/L citrate buffer （pH 4.5） at a dose of 55 mg/kg. Normal rats received an equal volume of citrate buffer. Three days post-STZ injection, tail vein blood glucose samples were collected and measured with Onetouchglucometer （Johnson & Johnson, USA）. The rats were considered diabetic and used for the study only if their glucose levels were greater than 15 mmol/L. Rats were housed 8 weeks after vehicle or STZ injection.

Abstract:Aim To study the effect of calcitriol for leukoaraiosis（LA） patients with mild cognitive impairment（MCI）. Methods 256 patients with LA, 181 patients with MCI were selected according to the diagnosis of MCI, and divided into two groups: control group （85 cases）, intervention group （88 cases）. Calcitriol 0.25 μg/day was used in intervention group, other treatments and rehabilitation treatment were the same in two groups. Observation period to two groups was 12 months. And cognitive function was test by montreal cognitive assessment （MoCA） score before include and 6 months and 12 months before and after treatment. The changes of cognitive function were comparatively analysed before and after treatment between the two groups. Results （1） 181 cases were diagnosed as MCI （70.70%） in 256 patients with LA, which were randomly divided into control group and intervention group, and got follow-up of 12 months 173 cases were into the statistics eventually, 85 cases in control group, 88 cases in intervention group All the patients into research had not appeared severe adverse reactions. （2） The delayed memory score was the lowest in two groups, and abstract feature, visual space and executive function were reduced significantly. MoCA score improvement was not obvious in intervention group at 6th month （19.23±2.42）, but the score increased from 18.84±2.08 before treatment to 22.32±2.36 at 12th month （P<0.01）, when the scores between two groups were different significantly （P<0.01）. The score of language increased in intervention group at 6th month, 12th month （2.37±0.86, 2.52±0.86）, compared with that of before intervention（1.84±0.73, P<0.01）. And at the two points, the language scores in intervention group were also different significantly compared with control group. For delayed memory, there were no obvious improvement in intervention group at 6th month （1.35+1.37）, but the score increased at 12th month （2.77±1.84） compared with that before intervention （1.30±1.41, P<0.01）. At 12th month the delayed memory scores were significantly different between two groups （1.41±1.46 vs 2.77±1.84, P<0.01）. The abstract function, visual space and executive function score in two groups had no significant change at each time point （P>0.05）. Conclusions The calcitriol was effective on MCI correlation with LA, but the work was slow. The language ability improved faster, and delay memory function needed a long treatment cycle. It had a certain limitation for calcitriol to improve the abstract function, visual space and executive function.

Abstract:Aim To analyze the risk factors for triple-vessel coronary artery disease between different genders. Methods A total of 1 262 patients （907 males and 355 females）, who underwent coronary angiography and were diagnosed coronary heart disease, and their gender ,ages, hypertension, total cholesterol（TC）, triglycerides（TG）, low-density lipoprotein cholesterol （LDLC）, high-density lipoprotein cholesterol （HDLC）, uric acid（UA）, diabetes and smoking history were recorded. First, all cases were divided into two groups according to whether triple-vessel disease or not. Risk factors were compared between the two groups. Then they were further divided into groups based on gender, the risk factors between triple-vessel coronary artery disease and non-triple-vessel coronary artery disease in males and females were compared respectively. Results Univariate analysis showed that the age, male ratio, TC, LDLC, UA, hypertension ratio, diabetes ratio, smoking ratio of triple-vessel coronary artery disease were higher than non-triple-vessel coronary artery disease. The HDLC of triple-vessel coronary artery disease was lower than non-triple-vessel coronary artery disease. And the difference was statistically significant（P<0.05）. For males, the age, TC, LDLC, UA, diabetes ratio of triple-vessel coronary artery disease were higher than non-triple-vessel coronary artery disease. The HDLC of triple-vessel coronary artery disease was lower than non-triple-vessel coronary artery disease. And the difference was statistically significant（P<0.05）. For female, the age, LDLC, hypertension ratio, diabetes ratio of triple-vessel coronary artery disease were higher than non-triple-vessel coronary artery disease. The HDL-C of triple-vessel coronary artery disease was lower than non-triple-vessel coronary artery disease. And the difference was statistically significant（P<0.05）. Logistic regression analysis showed that the most significant risk factor for triple-vessel coronary artery disease were diabetes. Conclusion

Abstract:Aim Epigenetic features such as DNA methylation are increasingly being recognized as an important factor in the occurrence of many complex diseases. However, there are limited data on the DNA methylation changes in ischemic stroke patients. This study is designed to determine whether the DNA methylation status of estrogen receptor-α （ER-α） gene promoter is related to ischemic stroke. Methods 83 ischemic stroke patients and 94 control subjects were selected for research. The infarct size was recorded and the severity of neurological impairment was assessed by National Institute of Health Stroke Scale （NIHSS） and Barthel Index. For patients with carotid artery color Doppler ultrasound and brain magnetic resonance angiography （MRA）, Crouse score and plaque index were calculated to evaluate the severity of intracranial atherosclerosis. Morning fasting venous blood sample was taken for DNA extraction. The methylation status of ER-α gene promoter was measured by methylation specific polymerase chain reaction （MSP）. Results The ER-α gene promoter methylation frequency was higher in ischemic stroke group than in control group （42.2% vs 19.1%, P＜0.05）. Carotid artery color ultrasound examination was performed in 52 patients, and there were statistical differences in carotid intima-media thickness （CIMT）, Crouse score and plaque index among full-methylation, part-methylation and non-methylation subgroups （P＜0.05）. Brain MRA was performed in 57 patients, and the methylation frequency had tendency to increase with the severity of intracranial atherosclerosis （respectively 40.9%, 42.9%, 52.4%, 57.1%）, but there was no statistical significance （P>0.05）. According to the size of infarct, the patients was divided into small infarction group, middle infarction group and large infarction group, and methylation frequency increased in turn （respectively 32.8%, 56.3%, 77.8%）, the difference was statistically significant （P＜0.05）. There were statistical differences in NIHSS score and Barthel index among full-methylation, part-methylation and non-methylation subgroups （P＜0.05）. Conclusions The ER-α gene promoter methylation frequency is higher in ischemic stroke patients than in control group. The ER-α gene promoter methylation status is related to the severity of carotid atherosclerosis, infarct size and the severity of neurological impairment.

Abstract:Aim To analyse the value of application and influence factors of pulse wave velocity （PWV）. Methods A total of 164 patients were divided into four groups: normal group, hypertensive group（HP）, coronary heart disease group（CHD） and coronary heart disease with hypertensive group（CHD+HP）. All patients were underwent coronary angiography（CAG）. Meanwhile, PWV were measured by invasive methods. Other baseline data, such as gender, age, height, weight and blood lipid, uric acid, creatinine and homocysteine were measured at the same time. One-way ANOVA, multiple linear regression and q tests were used in this study. Results （1） There were significant difference in carotid-femoral pulse wave velocity（CFPWV） and carotid-dorsal artery of foot pulse wave velocity （CDPWV） among those four groups. CFPWV and CDPWV of those three groups were significantly higher than that of normal group. There was no significant difference in carotid-radial pulse wave velocity （CRPWV） among those four groups. （2）There was no significantly difference in CFPWV and CDPWV between HP group and pure CHD group. CFPWV of CHD+HP group was significant higher than that of HP group and pure CHD group（P<0.05）. CDPWV of CHD+HP group was significantly higher than that of pure CHD group（P<0.05）. （3）There was significant difference in CFPWV, CDPWV and CFPWV for within-group. （4）Multiple stepwise linear regression analysis found that heart rate, homocysteine, high density lipoprotein cholesterol （HDLC） and pulse pressure（PP） were predisposed factors for CFPWV, while HDLC and mean artery pressure（MAP） were predisposed factors for CDPWV. Conclusion PWV was higher in patients with hypertension and coronary heart disease than that of normal people. Vascular injury of patients with CHD complicated HP is significantly more severe than that of HP or pure CHD. CFPWV has higher clinical value in daily practice. Heart rate, blood pressure, plasma homocysteine and HDLC were the influence factors of the PWV. PWV provides reliable reference index for early prevention, diagnosis and treatment of hypertension and coronary heart disease.

Abstract:Aim To investigate the value of dual-source 256 slice spiral CT dual-energy scanning in diagnosis of aortic intramural hematoma （AIH）. Methods AIH CT imaging data were retrospectively reviewed from Oct 2012 to Aug 2014. 41 patients with AIH were diagnosed by dual-source 256 slice spiral CT dual-energy scanning. The original data were processed by image postprocessing technology, including virtual non-contrast （VNC）, multi-planar reconstruction （MPR）, curved planar reconstruction （CPR）, and maximum intensity projection （MIP）. Results AIH caused aortic wall thickening, and all thicken aorta walls were more than 5 mm. There were 39 cases of crescent-thicken and 2 cases of circular-thicken. The aortic wall calcified plaque could be seen in 30 cases of patients, and within-shifted calcified plaque could be seen in 25 cases of patients. There were 32 cases with ulcer niche and 3 cases with lining leakage in the aortic wall. But no intimal tear crevasse could be found in all patients. In addition, there were 8 cases with simple pleural effusion, and 2 cases with pleural effusion and pericardial effusion. Conclusions AIH can be diagnosed fast, accurately, and noninvasively by dual-source 256 slice spiral CT dual-energy scanning. Dual-source 256 slice spiral CT dual-energy scanning can provide important information for constituting clinical reasonable treatment scheme.

Abstract:Aim To study the association between H-type hypertension and coronary slow flow （CSF） in patients undergoing PCI therapy with acute myocardial infarction. Methods 120 patients with hypertension and acute myocardial infarction which accepted the emergency treatment of PCI in our hospital from January 2013 to July 2014 were enrolled as the research subjects. According to the blood flow level presented during the PCI therapy, these cases were divided into CSF group （27 cases） and non-CSF group （93 cases）. Blood lipid level, high sensitivity C-reactive protein （hs-CRP） and plasma homocysteine were tested and compared between the two groups, so did the proportion of patients with H-type hypertension. The risk factors of CSF were screened by Logistic regression analysis. Results In CSF group, the proportion of patients with H-type hypertension was significantly higher than that in non-CSF group （P<0.05）. With Logistic regression analysis, H-type hypertension was found to be a significant risk factor of CSF. Conclusion H-type hypertension is closely related to the CSF in patients with acute myocardial infarction which undergo primary PCI treatment.

Abstract:Aim To investigate the correlation between lipoprotein（a）（Lp（a））,fibrinogen（FIB） and carotid atherosclerosis（CAS） in patients with chronic kidney disease （CKD）. Methods 348 cases of CKD were divided into 4 groups according to the intima-media thickness by carotid ultrasonography, and the normal control group was included in this study. The correlation between Lp （a）, FIB level and the degree of CAS was analysed. Results In patients with CKD, the serum level of Lp（a） and FIB increased gradually with the severity of atherosclerosis, the difference was statistically significant （P<0.01）. Serum Lp（a） and FIB levels were positively correlated with atherosclerosis by Spearson correlation analysis（r0.233,P<0.01r0.315,P<0.01）. Lp（a） and FIB were positively correlated to each other（r0.156，P<0.01）. Both Lp（a） and FIB were associated with CAS by Logistic regression analysis（P<0.05）.

Abstract:Aim To detect the correlation between hyperuricemia （HUA） and chronic heart failure. Methods We selected 422 patients with CHF （260 with HFpEF） and 134 patients without CHF hospitalized in Shengjing Hospital of China Medical University between February 2009 and January 2012. The correlation between HUA and CHF was analyzed with t inspection, χ² inspection and Logistic analysis and the prognostic correlation between them was further explored through Follow-up studies. Results Serum UA in HFpEF and HFrEF group （374.54±144.30 μmol/L, 416.45±168.93 μmol/L） was significantly higher than non-heart failure group （299.71±114.36 μmol /L, P<0.05）.

Abstract:Aim To explore the changes of plasma von willebrand factor （vWF） and von willebrand factor-cleaving protease （ADAMTS13） antigen levels in acute cerebral infarction （ACI） and the relationship between these changes and prognosis of ACI. Methods This was a case-control study, patients who received treatment were included. 64 patients with ACI were enrolled as the cases, 24 healthy persons were enrolled as the controls. The expression of plasma vWF and ADAMTS13 levels in patients and controls were measured by enzyme linked immunosorbent assay（ELISA）. All patients were followed up to evaluate mRS score of 90-day. The correlation was analysed by Pearson correlation analysis.

Abstract:Aim To detect the plasma levels of asymmetric dimethylarginine （ADMA） in patients with cerebral infarction （CI） To analyze the relations between ADMA and CI, other traditional risk factors of CI To explore the role of ADMA in the pathogenesis of CI. Methods 100 patients with CI were collected （CI group）, and 80 healthy examination individuals were as the control group. Plasma level of ADMA was determined by high performance liquid chromatography in the two groups. Fasting blood glucose, lipids and blood pressure in a calm state were measured at the same time.

Abstract:Aim To evaluate the association of apolipoprotein B （ApoB） EcoRI polymorphisms with coronary heart disease （CHD） in Chinese population by using a meta-analysis. Methods Hardy-Weinberg equilibrium （HWE） test was used to check genetic equilibrium among genotypes for the selected articles. A fixed or random effect model was selected based on a heterogeneity test. Publication bias was quantified and tested with Begg’s rank correlation method and/or Egger’s linear regression. This meta-analysis was conducted by using Stata 12.0 software. Results Ten reports that met the inclusion criteria were utilized for this meta-analysis. The results of meta-analysis indicated that the pooled OR（95%CI）of E⁺ vs E^-was 1.29 （1.04～1.60）, and P<0.05, the pooled OR（95%CI）of E⁺E⁺ vs E⁺E^- + E^-E^- was 1.28 （1.02～1.61）, and P<0.05. Conclusion In Chinese population, ApoB XbaI locus is an important susceptibility site for CHD.

Abstract:The lectin-like oxidized low density lipoprotein receptor-1 （LOX-1） on the vascular endothelial cell is the main receptor for oxidized low density lipoprotein. The extracellular domain of LOX-1 on the cell surface can undergo proteolysis and be released as soluble LOX-1 （sLOX-1）. The level of sLOX-1 in serum elevates for relative disease with atherosclerosis and vascular endothelium injuries, which suggests sLOX-1 is a promising biomarker. In the present paper the cardiovascular related diseases regarding sLOX-1 as biomarker were firstly reviewed in detail.

Abstract:Neurite outgrowth inhibitor （Nogo）, also known as reticulon-4 （RTN-4）, is mainly located in the endoplasmic reticulum, its gene encoding three kinds of products, namely Nogo-A, Nogo-B and Nogo-C. Nogo-A and Nogo-C are mainly involved in the inhibition of axonal regeneration after central nervous system injury. Because of Nogo-B’s being widely distributed, it not only affects the central nervous system regeneration, but also participates in the process of atherosclerosis, vascular endothelial regeneration, repair of the tissue damage and cell apoptosis. Nogo-B receptor （NgBR） is a specific receptor of Nogo-B N-terminal, and it can interact with Nogo-B or play a biological role independently. In recent years, it has been found that NgBR can be involved in the metabolism of cholesterol, the synthesis of alcohol, and the promotion of angiogenesis and the chemotaxis of endothelial cells. The biological function of NgBR is being paid more and more attention, and the research of NgBR in recent years is reviewed.

Abstract:As a new kind of biomarker, the decreased numbers of endothelial progenitor cells can predict the high incidence of cardiovascular events. Nowadays exercise rehabilitation has become a research hotspot, since it can reduce the morbidity of cardiovascular disease and improve the patients’ quality of life. Multiple evidence has demonstrated that cardiovascular rehabilitation can mobilize the endothelial progenitor cells and improve endothelia function,but the mechanism of mobilization is not fully understood，which seems to be closely related to the ischemic stimulation and the regulation of important humoral factors. This review will summarize the effects of exercise training on mobilization of endothelial progenitor cells in patients with cardiovascular disease and discuss the possible mechanisms involved.

Abstract:Cervical artery dissection （CeAD） is a major cause of ischemic stroke in young and middle-aged adults,although relatively uncommon in the community. Recent large collaborative projects have provided new insights into mechanisms and risk factors of CeAD. Pathologic changes observed at the media-adventitia border in temporal arteries of CeAD patients suggest a predisposing arterial wall weakness. In large multicenter series of CeAD patients, compared with agematched healthy controls and patients with an ischemic stroke of another cause, hypertension and migraine, especially without aura, were confirmed as risk factors for CeAD, in addition to cervical trauma and recent infection. Hypercholesterolemia and being overweight were shown to be inversely associated with CeAD. Differences in risk factor profile and structural features between carotid and vertebral dissection suggest that their pathophysiology may partly differ. An association of CeAD with fibromuscular dysplasia and reversible cerebral vasoconstriction syndrome was described. Genetic risk factors of CeAD are still poorly understood. Large cohorts of CeAD patients have refined our understanding of the pathophysiology and risk factors of CeAD, but the molecular mechanisms are still poorly understood. Ongoing high-throughput genetic projects will hopefully provide novel insight into the biological substrate of CeAD.